The intersection of lung and the intersection of fiber and cause of disease of taking of sending etc. specially and have illness coming on the intersection of mechanism and the intersection of _ and general knowledge

The intersection of lung and the intersection of fiber and cause of disease of taking of sending etc. specially and have illness coming on the intersection of mechanism and the intersection of _ and general knowledge
IPF cause of disease is not clear, mechanism has not also totally expounded the onset, but already enough evidences have indicated to relate to the fact that immune inflammation has been damaged. The inflammatory response characteristic of immunity that different samples reveal is not the same, what the blood around reflected is that immunity is unusual more outstanding, and the bronchus alveolus irritates lotion to reveal inflammation reacts for the main fact, and the abnormal state of lung local organization is different to some extent. So it studies materials to need to consider this kind of difference to assess various.
Synthesize the research in recent years, have illness coming on about IPF mechanism and course summarize as follows: A certain unknown antigen activates B cells, produce Ig and and form the immune complex, and then stimulate and activate alveolus macrophages. This immunoreaction is some in the lung, if alveolus wall B lymphocytes produced antibodies, then some compositions of the alveolus wall may be discerned as foreign matter wrongly. So someone thinks IPF can be regarded as one's own immune disease. But change and function of IPF patient T cells are indeterminate, only B cells are participated in not enough to prove it as one's own immune disease. Activatory alveolus macrophages release many kinds of mediums, damage structure such as the ground substance, basilar membrane of lung cells, cells directly except protein hydrolase, collagenase, reactive oxygen supersession product and some cell factors, still there is medium including fiber that is formed and closely related with with the fiber that connects albumens (fibronectin, FN) , the original growth factor (alveolarmacrophagederivedgrowthfactor hfactor, AMDGF) of macrophage of alveolus , the blood platelet derives growth factor (plateletderivedgrowthfactor, PDGF) With one kind of growth factors(insulinlikegrowthfactor, IGF) of insulin Wait, they can absorb into fibrous cells, and stimulate its hyperplasia, and lie between and lead the collagenic ground substance to shrink. IL-8, TNF,etc. released in alveolus macrophages lie between, lead, lay neutral cells to hasten and melt, assemble and activate towards the alveolus, form and increase by neutral grains of cell rate (20%) It is alveolus inflammation of the characteristic, and neutral grains of cell inflammation react and release a series of medium again, cause or aggravate the lung to damage with the fiber. Become hyperplasia of fibrous cell and produce important link and result that the glue was a disease. Normal people become fibrous cell grow have accurate adjustment, the intersection of prostaglandin and E2 for instance, become fibrous cell move, inhibit factor,etc. from belong to and shoulder and regulate the factor. In addition find a kind of C-sis gene which encodes PDGF in IPF, very similar to shifting virus cancer genetic V-sis. So emergence of IPF represent, succeed fibrous defeat of cell regulate, fail, or become fibrous cell " Tumour " Hyperplasia is a question very full of interest. Though someone finds the aggregate velocity or total amount that the quality is collagenic has not increased among IPF patient's lung, but type increase collagen, type rise collagen getting more collagenic for 2 type rate. Because type glue to be high in every one tension intensity, low to last sex, last one that arrange parallelly to cross by fibers belt, increasing shape and physiology sufficient to explain IPF to change of it, and no matter the collagenic total amount increases or not.
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